Intraganglionic laminar endings (IGLEs) are vagal afferent nerve terminals that wrap around the gastric muscle wall and act as tension receptors. Distension of the stomach stretches the terminal membrane and gates mechanosensitive Piezo2 channels. Channel open probability follows a Boltzmann relation in stretch λ:
P_open(λ) = 1 / (1 + exp(-(λ - λ½) / k))
V_gen = V_max · P_open (graded receptor / generator potential)
The generator potential does not travel far on its own — once it depolarizes the terminal past threshold, voltage-gated Na⁺ channels fire a train of all-or-none action potentials. The stomach does not encode "how full" in the potential's amplitude, but in the rate of that train — a Hill-type stimulus–response curve seen in real single-unit vagal afferent recordings:
f(S) = f_max · Sⁿ / (Kₘⁿ + Sⁿ) S = normalized wall stretch, n ≈ 2
- Gastric fill — sets wall stretch S directly, as a meal would.
- CCK / satiety hormone — cholecystokinin, released by duodenal cells in response to fat and protein, sensitizes the same afferents by lowering Kₘ, so the same stretch fires faster (a real vago-humoral synergy, not two separate channels).
- Slowly-adapting vs rapidly-adapting — IGLEs are slowly-adapting tension receptors that keep firing steadily for as long as the wall stays stretched, encoding sustained fullness; intramuscular array (IMA) afferents are rapidly-adapting and fire mainly on the transient of a contraction or a stretch change, then decay back toward baseline.
- Vagotomy — severing the nerve abolishes the ascending signal entirely regardless of stretch, which is exactly why surgical/pharmacological vagal blockade is studied as a satiety and obesity intervention.
The resulting spike train travels up the vagus nerve to the nucleus tractus solitarius (NTS) in the brainstem — the first synaptic relay of the gut-brain axis for gastric mechanical signals, upstream of the hypothalamic circuits that shape meal termination.